HUMAN HERPESVIRUS 6B INFECTION AND THYROID AUTOIMMUNITY – MOLECULAR AND IMMUNOLOGICAL INVESTIGATION OF THE ASSOCIATION.

Human herpesvirus 6 (HHV-6) is an ever-present human pathogen that can persist in its host indefinitely. Even though the primary infection is most often mild, HHV-6 has been linked with several disease development later in life, especially autoimmune. HHV-6 is considered an environmental autoimmunity-triggering factor, and associations between the virus and several autoimmune conditions have been made. We aimed to demonstrate the link between HHV-6 and thyroid autoimmunity via molecular and immunological investigations of samples obtained from patients with autoimmune thyroiditis (AIT). Postoperative thyroid tissues and whole blood from 119 AIT patients were collected. Nucleic acids were isolated from thyroid tissue samples and whole blood and used for HHV-6 DNA, active infection marker detection, and load determination.
Blood plasma from 81 patients was used for HHV-6 protein-specific antibody detection. FFPE tissues from 4 patients were used for immunofluorescent microscopy. All patients harboured HHV6 in their thyroids with a median viral load of 558,3 HHV-6 copies/106 cells, in one patient reaching 1883419,8 HHV-6 copies/106 cells. Twenty patients had detectable HHV-6 in the blood, yet with
extremely low viral loads – 4,1 HHV-6 copies/106 cells. In 55 thyroid tissues, markers of active infection were found. We evaluated the potential role of two poorly studied HHV-6 proteins (U12 and U51) in thyroid autoimmunity – 36 tissues expressed the proteins, and in tissues expressing U12/U51, viral loads were significantly higher (1399 vs 238 HHV-6 copies/106 cells). U12 and
U51 antibodies could be detected in patient plasma and microscopy revealed the colocalization of HHV-6 glycoproteins and U12/U51. The high prevalence of HHV-6 in thyroid glands points to its role in AIT development or disease exacerbation. HHV-6 U12/U51 may help HHV-6 evade immune responses and persist in the thyroid.